Journals / Turkish Journal of Gastroenterology / 2014 / Cilt: 25 - Sayı: 6

No association between the functional cannabinoid receptor type 2 Q63R variants and inflammatory bowel disease in Turkish subjects

Pages
639–643
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusion: These pilot findings suggest that CB2 Q63R polymorphism does not play a major role in genetic susceptibility to IBD or in its disease phenotypes among Turkish subjects.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Background/Aims: The endocannabinoid system can exert beneficial effects on gastrointestinal inflammation, and cannabinoid receptor-2 (CB2) agonists may represent a new therapeutic approach in inflammatory bowel disease (IBD).
📊
Key Findings & Data:A functional CB2 Q63R polymorphism (rs35761398) in the CNR2 gene has been shown to affect the immunomodulating properties of the CB2 receptor.
💡
Conclusion & Impact:Conclusion: These pilot findings suggest that CB2 Q63R polymorphism does not play a major role in genetic susceptibility to IBD or in its disease phenotypes among Turkish subjects.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Özet

Background/Aims: The endocannabinoid system can exert beneficial effects on gastrointestinal inflammation, and cannabinoid receptor-2 (CB2) agonists may represent a new therapeutic approach in inflammatory bowel disease (IBD). A functional CB2 Q63R polymorphism (rs35761398) in the CNR2 gene has been shown to affect the immunomodulating properties of the CB2 receptor. We sought to investigate whether the functional CB2 Q63R polymorphism (rs35761398) is associated with IBD susceptibility in a Turkish clinical sample. Materials and Methods: A total of 202 IBD patients, comprising 101 Crohn's disease (CD) patients and 101 ulcerative colitis (UC) patients, and 101 healthy controls were included in the study. The CB2 Q63R polymorphism was genotyped using real-time PCR. Results: There were no significant differences in the genotype frequencies of the three study groups. The odds ratio of the minor Q allele for CD relative to the common R allele was not significant (OR =1.02, 95% CI =0.67-1.56, p=0.99). Similarly, the odds ratio of the minor Q allele for UC relative to the common R allele did not reach statistical significance (OR =1.10, 95% CI =0.72-1.68, p=0.75). Moreover, the genotype frequencies did not show any significant association with the disease extent in either CD (p= 0.71) or UC patients (p=0.59). Conclusion: These pilot findings suggest that CB2 Q63R polymorphism does not play a major role in genetic susceptibility to IBD or in its disease phenotypes among Turkish subjects.

🔖

Cite This Article

YONAL, O., EREN, F., YILMAZ, Y., ATUĞ, Ö., ÖVER, H. H. (2014). No association between the functional cannabinoid receptor type 2 Q63R variants and inflammatory bowel disease in Turkish subjects. Turkish Journal of Gastroenterology, Cilt: 25 - Sayı: 6, 639–643. https://ajindex.com/articles/409543

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (20)

  1. Maher MM. Inflammatory bowel disease: review and future view. Front Biosci (Elite Ed) 2012; 4: 1638-47
  2. Glick SR, Carvalho RS. Inflammatory bowel disease. Pediatr Rev 2011;32: 14-24
  3. Hanauer SB. Inflammatory bowel disease: epidemiology, pathogenesis, and therapeutic opportunities. Inflamm Bowel Dis 2006;12: S3-9
  4. Baumgart DC, Sandborn WJ. Crohn's disease. Lancet 2012; 380: 1590-605
  5. Hovde Ø, Moum BA. Epidemiology and clinical course of Crohn's disease: results from observational studies. World J Gastroenterol 2012; 18: 1723-31
  6. Ford AC, Moayyedi P, Hanauer SB. Ulcerative colitis. BMJ 2013; 346: f432
  7. Ordás I, Eckmann L, Talamini M, et al. Ulcerative colitis. Lancet 2012; 380: 1606-19
  8. Khor B, Gardet A, Xavier RJ. Genetics and pathogenesis of inflammatory bowel disease. Nature 2011; 474: 307-17
  9. Xavier RJ, Podolsky DK. Unravelling the pathogenesis of inflammatory bowel disease. Nature 2007; 448: 427-34
  10. Basu D, Lopez I, Kulkarni A, et al. Impact of race and ethnicity on inflammatory bowel disease. Am J Gastroenterol 2005; 100: 2254-61
  11. Farrokhyar F, Swarbrick ET, Irvine EJ.A critical review of epidemiological studies in inflammatory bowel disease. Scand J Gastroenterol 2001; 36: 2-15
  12. Orholm M, Fonager K, Sørensen HT. Risk of ulcerative colitis and Crohn's disease among offspring of patients with chronic inflammatory bowel disease. Am J Gastroenterol 1999; 94: 3236-8
  13. Graham ES, Ashton JC, Glass M. Cannabinoid receptors: a brief history and "what's hot". Front Biosci 2009; 14: 944-57
  14. Console-Bram L, Marcu J, Abood ME. Cannabinoid receptors: nomenclature and pharmacological principles. Prog Neuropsychopharmacol Biol Psychiatry 2012; 38: 4-15
  15. Howlett AC, Blume LC, Dalton GD. CB(1) cannabinoid receptors and their associated proteins. Curr Med Chem 2010; 17: 1382-93
  16. Izzo AA. The cannabinoid CB(2) receptor: a good friend in the gut. Neurogastroenterol Motil 2007; 19: 704-8
  17. Di Marzo V, Izzo AA. Endocannabinoid overactivity and intestinal inflammation. Gut 2006; 55: 1373-6
  18. D'Argenio G, Valenti M, Scaglione G, et al. Up-regulation of anandamide levels as an endogenous mechanism and a pharmacological strategy to limit colon inflammation. FASEB J 2006; 20: 568-70
  19. Wright K, Rooney N, Feeney M, et al. Differential expression of cannabinoid receptors in the human colon: cannabinoids promote epithelial wound healing. Gastroenterology 2005; 129: 437-53
  20. Ihenetu K, Molleman A, Parsons ME, et al.